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Journal articles on the topic 'Bradykinina'

Author: Grafiati

Published: 24 April 2022

Last updated: 30 July 2025

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1

Śliż, Daniel. "Kiedy z punktu widzenia internisty warto zastosować acemetacynę?" Medycyna Faktów 16, no. 2(59) (2023): 204–7. http://dx.doi.org/10.24292/01.mf.0223.11.

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Niesteroidowe leki przeciwzapalne są powszechnie stosowane w łagodzeniu bólu i stanów zapalnych w różnych schorzeniach. Częstość i nasilenie bólu wzrastają wraz z wiekiem, co sprawia, że osoby starsze są bardziej zależne od leczenia przeciwbólowego. Celem tego podsumowania jest przedstawienie skuteczności i profilu bezpieczeństwa acemetacyny w porównaniu z innymi niesteroidowymi lekami przeciwzapalnymi.Acemetacyna wyróżnia się dobrym profilem bezpieczeństwa i skutecznością w łagodzeniu bólu i stanów zapalnych. Oprócz hamowania COX-1 i COX-2 lek ten wpływa również na mediatory stanu zapalnego,

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2

Przewłocka, Barbara, and Joanna Starnowska-Sokół. "Novel hybrid compounds designed by Polish scientists provide a long-lasting analgesic effect in a mouse model of neuropathic pain." BÓL 20, no. 2 / Zjazd PTBB (2019): 1–3. http://dx.doi.org/10.5604/01.3001.0013.4610.

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W polskich i niektórych europejskich mediach pojawiło się w ostatnim okresie wiele informacji na temat opracowanej przez polskich naukowców nowej substancji proponowanej jako lek przeciwbólowy. Ze względu na fakt, że badania te prowadzone były pod moim kierunkiem, podjęłam decyzję, aby czytelnikom kwartalnika „Ból” umożliwić zapoznanie się z genezą i wynikiem tych badań. Punktem wyjścia do wyżej wspomnianych badań, przeprowadzonych w Zakładzie Farmakologii Bólu Instytutu Farmakologii im. J. Maja Polskiej Akademii Nauk, była obserwacja, że po wielokrotnym podawaniu opioidów rozwija się toleranc

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3

Willars, Gary B., Werner Müller-Esterl, and Stefan R. Nahorski. "Receptor phosphorylation does not mediate cross talk between muscarinic M3 and bradykinin B2 receptors." American Journal of Physiology-Cell Physiology 277, no. 5 (1999): C859—C869. http://dx.doi.org/10.1152/ajpcell.1999.277.5.c859.

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This study examined cross talk between phospholipase C-coupled muscarinic M3 and bradykinin B2 receptors coexpressed in Chinese hamster ovary (CHO) cells. Agonists of either receptor enhanced phosphoinositide signaling (which rapidly desensitized) and caused protein kinase C (PKC)-independent, homologous receptor phosphorylation. Muscarinic M3 but not bradykinin B2 receptors were also phosphorylated after phorbol ester activation of PKC. Consistent with this, muscarinic M3 receptors were phosphorylated in a PKC-dependent fashion after bradykinin B2 receptor activation, but muscarinic M3 recept

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4

Ma, Jie, Yu Luo, Lilin Ge, et al. "Ranakinestatin-PPF from the Skin Secretion of the Fukien Gold-Striped Pond Frog,Pelophylax plancyi fukienensis: A Prototype of a Novel Class of BradykininB2Receptor Antagonist Peptide from Ranid Frogs." Scientific World Journal 2014 (2014): 1–9. http://dx.doi.org/10.1155/2014/564839.

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The defensive skin secretions of many amphibians are a rich source of bradykinins and bradykinin-related peptides (BRPs). Members of this peptide group are also common components of reptile and arthropod venoms due to their multiple biological functions that include induction of pain, effects on many smooth muscle types, and lowering systemic blood pressure. While most BRPs are bradykinin receptor agonists, some have curiously been found to be exquisite antagonists, such as the maximakinin gene-related peptide, kinestatin—a specific bradykinin B2-receptor antagonist from the skin of the giant

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5

Dixon, B. S., R. Breckon, J. Fortune, et al. "Effects of kinins on cultured arterial smooth muscle." American Journal of Physiology-Cell Physiology 258, no. 2 (1990): C299—C308. http://dx.doi.org/10.1152/ajpcell.1990.258.2.c299.

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The present study uses various kinin agonists and antagonists to examine the cellular mechanisms of bradykinin's actions on intracellular calcium, prostaglandins, and adenosine 3',5'-cyclic monophosphate (cAMP) accumulation in cultured arterial smooth muscle cells (casmc) obtained from rat mesenteric arteries. Exposure to bradykinin produced a rapid release of calcium (peak less than or equal to 20 s) from intracellular stores and an increase in prostaglandin (PG) E2 and cAMP production in casmc. Compared with bradykinin, the bradykinin B1-agonist [des-Arg9]BK produced only a small increase in

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6

Morgan-Boyd, R., J. M. Stewart, R. J. Vavrek, and A. Hassid. "Effects of bradykinin and angiotensin II on intracellular Ca2+ dynamics in endothelial cells." American Journal of Physiology-Cell Physiology 253, no. 4 (1987): C588—C598. http://dx.doi.org/10.1152/ajpcell.1987.253.4.c588.

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The purpose of this study was to investigate the effects of angiotensin II and bradykinin on intracellular Ca2+ dynamics in cultured endothelial cells. We used the "second-generation" fluorescent Ca2+ indicator fura-2, in conjunction with dual-wavelength fluorescence spectroscopy, in cultured adherent pulmonary arterial endothelial cells. Angiotensin II (up to 2 microM) had no consistent effect on intracellular Ca2+ levels. In contrast, bradykinin (10 nM) elicited a transient increase of cytosolic free Ca2+, from the resting value of 37 +/- 5 to 647 +/- 123 nM, followed by a decline to a stead

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7

Pan, H. L., C. L. Stebbins, and J. C. Longhurst. "Bradykinin contributes to the exercise pressor reflex: mechanism of action." Journal of Applied Physiology 75, no. 5 (1993): 2061–68. http://dx.doi.org/10.1152/jappl.1993.75.5.2061.

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This study determined the receptors responsible for mediating bradykinin's effect on skeletal muscle afferents that cause the pressor reflex in anesthetized cats. In eight cats, 1 microgram of bradykinin was injected intra-arterially into the gracilis muscle before and after intravenous injection of a kinin B2-receptor antagonist (NPC 17731, 20 micrograms/kg). Initial injection of bradykinin reflexly increased mean arterial pressure by 23 +/- 7 mmHg, maximal change in pressure over time by 439 +/- 272 mmHg/s, and heart rate by 11 +/- 4 beats/min. The hemodynamic response to bradykinin was abol

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8

CUGNO, Massimo, Francesco SALERNO, Jürg NUSSBERGER, Bianca BOTTASSO, Elettra LORENZANO, and Angelo AGOSTONI. "Bradykinin in the ascitic fluid of patients with liver cirrhosis." Clinical Science 101, no. 6 (2001): 651–57. http://dx.doi.org/10.1042/cs1010651.

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Bradykinin, a nonapeptide with vasodilatory and permeabilizing activity, is generated through the cleavage of high-Mr (‘high-molecular-weight’) kininogen by kallikrein, and its generation is facilitated by plasmin. In the ascitic fluid of patients with cirrhosis, there is massive cleavage of high-Mr kininogen and activation of fibrinolysis, but bradykinin has never been measured directly. In the ascitic fluid of 24 patients with cirrhosis, we measured bradykinin-(1-9)-nonapeptide levels by RIA after liquid-phase and subsequent HPLC extraction, and those of its catabolic product bradykininin-(1

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9

Gouda, Ahmed S., and Bruno Mégarbane. "Molecular Bases of Serotonin Reuptake Inhibitor Antidepressant-Attributed Effects in COVID-19: A New Insight on the Role of Bradykinins." Journal of Personalized Medicine 12, no. 9 (2022): 1487. http://dx.doi.org/10.3390/jpm12091487.

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Widely available effective drugs to treat coronavirus disease-2019 (COVID-19) are still limited. Various studies suggested the potential contribution of selective serotonin-reuptake inhibitor (SSRI) antidepressants to alleviate the clinical course of COVID-19. Initially, SSRI antidepressant-attributed anti-COVID-19 activity was attributed to their direct agonistic or indirect serotonin-mediated stimulation of sigma-1 receptors (Sig1-R). Thereafter, attention was drawn to the property of SSRI antidepressants to decrease ceramide production, as functional inhibitors of acid sphingomyelinase. Cer

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10

Todoriko, L. D. "Problem issues of the pathogenesis of inflammatory reaction and the course of coronavirus infection." Tuberculosis, Lung Diseases, HIV Infection, no. 1 (March 23, 2021): 76–86. http://dx.doi.org/10.30978/tb2021-1-76.

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Objective — to analysis and systematization of literature data about pathogenesis of the inflammatory reaction and the clinical course of coronavirus infection caused by SARS-CoV-2. Materials and methods. Access to various full-text and abstract databases was used for the search query «coronavirus», «COVID-19», «SARS-CoV-2» and their systematic evaluation was carried out. The most complete database of available literature sources (about 70) was obtainedon the molecular pathophysiology of COVID-19. Results and discussion. The results of the analysis of the molecular pathophysiology

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11

Krieg, Thomas, Qining Qin, Sebastian Philipp, Mikhail F. Alexeyev, Michael V. Cohen, and James M. Downey. "Acetylcholine and bradykinin trigger preconditioning in the heart through a pathway that includes Akt and NOS." American Journal of Physiology-Heart and Circulatory Physiology 287, no. 6 (2004): H2606—H2611. http://dx.doi.org/10.1152/ajpheart.00600.2004.

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In the rabbit heart, bradykinin and ACh trigger preconditioning by a mechanism involving ATP-sensitive potassium channel-dependent production of reactive oxygen species (ROS). Recent evidence indicates that the pathway by which bradykinin causes ROS generation includes nitric oxide synthase (NOS) and protein kinase G (PKG). On the other hand, Akt was shown to be essential for ACh to generate ROS. This study determines whether these two G-coupled receptor agonists indeed have similar signaling targets, i.e., whether Akt is involved in bradykinin's pathway and whether NOS is involved in ACh's pa

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12

Olson, K. R., D. J. Conklin, L. Weaver, et al. "Cardiovascular effects of homologous bradykinin in rainbow trout." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 272, no. 4 (1997): R1112—R1120. http://dx.doi.org/10.1152/ajpregu.1997.272.4.r1112.

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Bradykinins have only recently been identified in fish, and a detailed analysis of their cardiovascular actions is lacking. The present study examines the cardiovascular effects of trout bradykinin ([Arg0,Trp5,Leu8]bradykinin; tBK) in conscious trout, Oncorhynchus mykiss. tBK (1-10 nmol/kg body wt bolus) produced triphasic pressor-depressor-pressor responses. In phase 1, cardiac output (CO), ventral aortic (P(VA)), dorsal aortic (P(DA)), and central venous pressure increased, whereas systemic (R(S)) and gill resistance (R(G)) were unchanged. In phase 2, R(G) increased, whereas R(S), CO, and he

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13

Leong, Patrick K. K., Yibin Zhang, Li E. Yang, Niels-Henrik Holstein-Rathlou, and Alicia A. McDonough. "Diuretic response to acute hypertension is blunted during angiotensin II clamp." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 283, no. 4 (2002): R837—R842. http://dx.doi.org/10.1152/ajpregu.00089.2002.

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Acute hypertension inhibits proximal tubule (PT) fluid reabsorption. The resultant increase in end proximal flow rate provides the error signal to mediate tubuloglomerular feedback autoregulation of renal blood flow and glomerular filtration rate and suppresses renal renin secretion. To test whether the suppression of the renin-angiotensin system during acute hypertension affects the magnitude of the inhibition of PT fluid and sodium reabsorption, plasma ANG II levels were clamped by infusion of the angiotensin-converting enzyme (ACE) inhibitor captopril (12 μg/min) and ANG II after pretreatme

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14

Öztürk, Yusuf, V. Melih Altan, Nuray Yıdızoğlu-Arı, and Orhan Altınkurt. "Bradykinin receptors in intestinal smooth muscles and their post-receptor events related to calcium." Mediators of Inflammation 2, no. 4 (1993): 309–15. http://dx.doi.org/10.1155/s0962935193000432.

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The effects of trifluoperazine and verapamil on bradykinin- and des-Arg9-bradykinin induced responses of isolated rat duodenum and guinea-pig ileum were investigated to elucidate post-bradykinin receptor events. Verapamil and trifluoperazine inhibited bradykinin induced relaxations and contractions and des-Arg9- bradykinin induced contractions in rat duodenum. Bradykinin induced contractions of ileum were also inhibited by trifluoperazine and. verapamil. Since non-competitive affinity constants of trifluoperazine and verapamil for the relaxant responses to bradykinin in duodenum and for the co

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15

Chen, Zu-Lin, Pradeep Singh, Jyen Wong, Katharina Horn, Sidney Strickland та Erin H. Norris. "An antibody against HK blocks Alzheimer’s disease peptide β-amyloid−induced bradykinin release in human plasma". Proceedings of the National Academy of Sciences 116, № 46 (2019): 22921–23. http://dx.doi.org/10.1073/pnas.1914831116.

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Bradykinin is a proinflammatory factor that mediates angioedema and inflammation in many diseases. It is a key player in some types of hereditary angioedema and is involved in septic shock, traumatic injury, Alzheimer’s disease (AD), and stroke, among others. Activation of the plasma contact system leads to elevated levels of plasma kallikrein, which cleaves high molecular weight kininogen (HK) to release bradykinin. Drug development for bradykinin-meditated pathologies has focused on designing inhibitors to the enzymes that cleave HK (to prevent bradykinin release) or antagonists of endotheli

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16

Duncan, Ann-Maree, Athena Kladis, Garry L. Jennings, Anthony M. Dart, Murray Esler, and Duncan J. Campbell. "Kinins in humans." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 278, no. 4 (2000): R897—R904. http://dx.doi.org/10.1152/ajpregu.2000.278.4.r897.

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The kinin peptide system in humans is complex. Whereas plasma kallikrein generates bradykinin peptides, glandular kallikrein generates kallidin peptides. Moreover, a proportion of kinin peptides is hydroxylated on proline3 of the bradykinin sequence. We established HPLC-based radioimmunoassays for nonhydroxylated and hydroxylated bradykinin and kallidin peptides and their metabolites in blood and urine. Both nonhydroxylated and hydroxylated bradykinin and kallidin peptides were identified in human blood and urine, although the levels in blood were often below the assay detection limit. Whereas

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17

HARVEY, Justine S., and Gillian M. BURGESS. "Cyclic GMP regulates activation of phosphoinositidase C by bradykinin in sensory neurons." Biochemical Journal 316, no. 2 (1996): 539–44. http://dx.doi.org/10.1042/bj3160539.

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Prior exposure of cultured neonatal rat dorsal root ganglion (DRG) neurons to bradykinin resulted in marked attenuation of bradykinin-induced activation of phosphoinositidase C (PIC). The (logconcentration)–response curve for bradykinin-induced [3H]inositol trisphosphate ([3H]IP3) formation was shifted to the right and the maximum response was reduced. Bradykinin increases cyclic GMP (cGMP) in DRG neurons [Burgess, Mullaney, McNeill, Coote, Minhas and Wood (1989) J. Neurochem. 53, 1212–1218] and treatment of the neurons with dibutyryl cGMP (dbcGMP) had a similar, inhibitory, effect on bradykin

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18

McAllister, B. S., F. Leeb-Lundberg, and M. S. Olson. "Bradykinin inhibition of EGF- and PDGF-induced DNA synthesis in human fibroblasts." American Journal of Physiology-Cell Physiology 265, no. 2 (1993): C477—C484. http://dx.doi.org/10.1152/ajpcell.1993.265.2.c477.

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Bradykinin exhibits proliferative influences in several types of cells; however, in the present study, bradykinin did not promote DNA synthesis but actually inhibited the DNA synthesis induced by epidermal growth factor (EGF) and platelet-derived growth factor (PDGF) in human gingival fibroblasts (HGF). This dose-dependent inhibitory effect was a specific intracellular interaction in that increasing concentrations of EGF did not counteract the inhibitory actions of bradykinin when added at 100 nM. The phosphoinositide-calcium signaling cascade is a likely point of interaction for the inhibitor

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Gauthier, Kathryn M., Cody J. Cepura, and William B. Campbell. "ACE inhibition enhances bradykinin relaxations through nitric oxide and B1 receptor activation in bovine coronary arteries." Biological Chemistry 394, no. 9 (2013): 1205–12. http://dx.doi.org/10.1515/hsz-2012-0348.

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Abstract Bradykinin causes vascular relaxations through release of endothelial relaxing factors including prostacyclin, nitric oxide (NO) and epoxyeicosatrienoic acids (EETs). Bradykinin is metabolized by angiotensin converting enzyme (ACE) and ACE inhibition enhances bradykinin relaxations. Our goal was to characterize the role of bradykinin receptors and endothelial factors in ACE inhibitor-enhanced relaxations in bovine coronary arteries. In U46619 preconstricted arteries, bradykinin (10-11-10-8m) caused concentration-dependent relaxations (maximal relaxation ≥100%, log EC50=-9.8±0.1). In t

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20

Asano, Masayuki, Hiroe Sawai, Chie Hatori, Noriaki Inamura, Tatsujiro Fujiwara, and Kunio Nakahara. "Effects of a nonpeptide bradykinin B2 receptor antagonist, FR167344, on guinea-pig tracheal smooth muscle bradykinin receptors." Canadian Journal of Physiology and Pharmacology 76, no. 10-11 (1998): 1051–55. http://dx.doi.org/10.1139/y98-098.

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It is speculated that bradykinin may play an important role in asthma. Thus, bradykinin receptor antagonists may have therapeutic potential against asthma. Orally active bradykinin antagonists would be more desirable for the treatment of the disease. In the present study, we examined the effects of a novel, potent, selective, and orally active nonpeptide bradykinin B2 receptor antagonist, FR167344 (N-[N-[3-[(3-bromo-2-methylimidazo[1,2-a]pyridin-8-yl)oxymethyl]- 2,4-dichlorophenyl]-N-methylaminocarbonylmethyl]-4-(dimethylaminocarbonyl)cinnamylamide hydrochloride), on guinea-pig tracheal smooth

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21

Grafe, M., C. Bossaller, K. Graf, et al. "Effect of angiotensin-converting-enzyme inhibition on bradykinin metabolism by vascular endothelial cells." American Journal of Physiology-Heart and Circulatory Physiology 264, no. 5 (1993): H1493—H1497. http://dx.doi.org/10.1152/ajpheart.1993.264.5.h1493.

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The degradation of bradykinin by angiotensin-converting-enzyme (ACE) activity in cultured human endothelial cells was studied by direct measurement of bradykinin and by its effect on the release of endothelium-derived relaxing factors. The half-life of exogenous bradykinin (10,000 pg/ml) was calculated from the decay of the bradykinin concentration as 46 +/- 2 min in cell monolayers, 133 +/- 15 min in conditioned medium, and 24 +/- 2 min in homogenates. Most of the bradykinin-degrading activity in cell monolayers could be inhibited in a concentration-dependent manner by the ACE inhibitors lisi

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22

Berman, A. R., A. G. Togias, G. Skloot, and D. Proud. "Allergen-induced hyperresponsiveness to bradykinin is more pronounced than that to methacholine." Journal of Applied Physiology 78, no. 5 (1995): 1844–52. http://dx.doi.org/10.1152/jappl.1995.78.5.1844.

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Bradykinin reduces airflow in asthmatic patients via indirect mechanism(s), possibly involving sensory nerve stimulation and increased vascular permeability. We hypothesized that allergen inhalation, which affects reactivity of nerves and vessels, would differentially alter reactivity to bradykinin and the smooth muscle spasmogen methacholine. We compared reactivity to methacholine and bradykinin 1, 2, 4, 7, 11, and 14 days after allergen provocation in 12 atopic asthmatic patients with stable baseline reactivity to bradykinin. Maximal allergen-induced shifts from baseline in reactivity were 0

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23

Kajekar, Radhika, and Allen C. Myers. "Effect of bradykinin on membrane properties of guinea pig bronchial parasympathetic ganglion neurons." American Journal of Physiology-Lung Cellular and Molecular Physiology 278, no. 3 (2000): L485—L491. http://dx.doi.org/10.1152/ajplung.2000.278.3.l485.

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The effect of bradykinin on membrane properties of parasympathetic ganglion neurons in isolated guinea pig bronchial tissue was studied using intracellular recording techniques. Bradykinin (1–100 nM) caused a reversible membrane potential depolarization of ganglion neurons that was not associated with a change in input resistance. The selective bradykinin B2 receptor antagonist HOE-140 inhibited bradykinin-induced membrane depolarizations. Furthermore, the cyclooxygenase inhibitor indomethacin attenuated bradykinin-induced membrane depolarizations to a similar magnitude (∼70%) as HOE-140. Howe

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24

SCHANSTRA, JOOST P., MARIA E. MARIN-CASTAÑO, FRANÇOISE PRADDAUDE, et al. "Bradykinin B1Receptor-Mediated Changes in Renal Hemodynamics during Endotoxin-Induced Inflammation." Journal of the American Society of Nephrology 11, no. 7 (2000): 1208–15. http://dx.doi.org/10.1681/asn.v1171208.

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Abstract. Kinins have been shown to influence renal hemodynamics and function. Under physiologic conditions, most kinin effects involve bradykinin B2receptors, but bradykinin B1receptors are often induced during inflammation. The purpose of this study was to examinein vivothe effects of bradykinin B1receptor activation on renal hemodynamics under normal and inflammatory conditions. In anesthetized rats, activation of bradykinin B1receptors by arterial infusion of bradykinin B1receptor agonist des-Arg9-bradykinin reduced renal plasma flow and GFR. Prior administration (18 h) of lipopolysacchari

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Bertrand, C., P. Geppetti, J. Baker, G. Petersson, G. Piedimonte, and J. A. Nadel. "Role of peptidases and NK1 receptors in vascular extravasation induced by bradykinin in rat nasal mucosa." Journal of Applied Physiology 74, no. 5 (1993): 2456–61. http://dx.doi.org/10.1152/jappl.1993.74.5.2456.

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We used Evans blue dye to assess the effects of bradykinin on vascular extravasation in nasal mucosa of pathogen-free F344 rats. There was a dose-dependent increase in Evans blue extravasation when bradykinin was delivered by topical instillation in the nose (doses, 25–100 nmol). Only the highest intravenous doses (2 and 5 mumol/kg) of bradykinin caused increased extravasation. When bradykinin was delivered by either route, its effect on extravasation was exaggerated by pharmacological inhibition of the enzymes neutral endopeptidase (NEP) and kininase II [angiotensin-converting enzyme (ACE)].

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Feletou, M., M. Germain, and B. Teisseire. "Converting-enzyme inhibitors potentiate bradykinin-induced relaxation in vitro." American Journal of Physiology-Heart and Circulatory Physiology 262, no. 3 (1992): H839—H845. http://dx.doi.org/10.1152/ajpheart.1992.262.3.h839.

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Experiments were designed to study the effects of converting-enzyme inhibitors (captopril and S 10211) on the endothelium-dependent relaxation to bradykinin in isolated porcine arteries. Rings of femoral arteries with and without endothelium were suspended in organ chambers to record isometric tension. Rings of coronary arteries without endothelium were used as bioassay tissue to record release of endothelium-derived relaxing factor (EDRF) from perfused femoral arteries. In organ chambers, bradykinin induced endothelium-dependent relaxation and, inconsistently, endothelium-independent contract

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Wilkes, B. M., and P. F. Mento. "Bradykinin-induced vasoconstriction and thromboxane release in perfused human placenta." American Journal of Physiology-Endocrinology and Metabolism 254, no. 6 (1988): E681—E686. http://dx.doi.org/10.1152/ajpendo.1988.254.6.e681.

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This investigation was performed to study the effects of bradykinin on the human fetoplacental circulation. The artery to a single placental cotyledon was perfused with RPMI medium (0.764 ml/min). Bradykinin caused a dose-related increase in vascular resistance. Because bradykinin is generally a vasodilator, we investigated the possibility that bradykinin-induced vasoconstriction was due to interactions with other pressor systems. Bradykinin and 9,11-dideoxy-9 alpha, 11 alpha-epoxymethanoprostaglandin F2 alpha (a stable thromboxane agonist) caused a dose-related increase in perfusion pressure.

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Yamawaki, I., P. Geppetti, C. Bertrand, B. Chan, and J. A. Nadel. "Airway vasodilation by bradykinin is mediated via B2 receptors and modulated by peptidase inhibitors." American Journal of Physiology-Lung Cellular and Molecular Physiology 266, no. 2 (1994): L156—L162. http://dx.doi.org/10.1152/ajplung.1994.266.2.l156.

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We studied the effect of exogenous bradykinin on blood flow in the airway microcirculation of anesthetized F344 rats in vivo. We made three successive determinations of airway blood flow and cardiac output using a modification of the reference sample microsphere technique. Injection of bradykinin into the left ventricle increased airway blood flow in a dose-related manner. Pretreatment with the bradykinin B2 receptor antagonist, Hoe 140, completely abolished bradykinin-, but not histamine-induced vasodilation. A bradykinin B1 receptor agonist, [des-Arg9]bradykinin, did not affect airway blood

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Polosa, R., K. Rajakulasingam, G. Prosperini, LV Milazzo, G. Santonocito, and ST Holgate. "Cross-tachyphylactic airway response to inhaled bradykinin, kallidin and [desArg9]-bradykinin in asthmatic subjects." European Respiratory Journal 6, no. 5 (1993): 687–93. http://dx.doi.org/10.1183/09031936.93.06050687.

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Kinins are oligopeptides that may act as mediators in the pathogenesis of bronchial asthma by interacting with specific cell surface receptors designated B1 and B2. When administered by inhalation to asthmatic subjects, bradykinin and kallidin, but not [desArg9]-bradykinin, provoke potent bronchoconstriction, thus suggesting a specific effect compatible with the stimulation of B2 receptors. To characterize further the receptor(s) mediating this bronchospastic response we have carried out cross-tachyphylactic studies with inhaled bradykinin, kallidin, and [desArg9]-bradykinin, administered in a

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Yang, C., and W. H. Hsu. "Stimulatory effect of bradykinin on insulin release from the perfused rat pancreas." American Journal of Physiology-Endocrinology and Metabolism 268, no. 5 (1995): E1027—E1030. http://dx.doi.org/10.1152/ajpendo.1995.268.5.e1027.

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Rat pancreas perfusion was performed to study the effect of bradykinin on insulin release. At the perfusate glucose concentration of 6 mM, bradykinin (0.01-1 microM) increased insulin release in a concentration-dependent manner. In addition, bradykinin (1 microM) increased the glucose (10 mM)-induced insulin release. HOE-140 (0.1 microM), a bradykinin B2-receptor antagonist, decreased the baseline insulin release and abolished the bradykinin (1 microM)-induced increase in insulin release. In addition, HOE-140 (0.1 microM) attenuated the glucose (10 mM)-induced increase in insulin release. Beca

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Bhoj, Priyanka S., Cassandra Nocito, Namdev S. Togre, et al. "Tissue Kallikrein-1 Suppresses Type I Interferon Responses and Reduces Depressive-Like Behavior in the MRL/lpr Lupus-Prone Mouse Model." International Journal of Molecular Sciences 25, no. 18 (2024): 10080. http://dx.doi.org/10.3390/ijms251810080.

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Excessive production and response to Type I interferons (IFNs) is a hallmark of systemic lupus erythematosus (SLE). Neuropsychiatric lupus (NPSLE) is a common manifestation of human SLE, with major depression as the most common presentation. Clinical studies have demonstrated that IFNα can cause depressive symptoms. We have shown that the kallikrein–kinin system (KKS) [comprised of kallikreins (Klks) and bradykinins] and angiotensin-converting enzyme inhibitors suppressed Type I IFN responses in dendritic cells from lupus-prone mice and human peripheral blood mononuclear cells. Tissue Klk gene

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GRANESS, Angela, Sabine HANKE, Frank D. BOEHMER, Peter PRESEK, and Claus LIEBMANN. "Protein-tyrosine-phosphatase-mediated epidermal growth factor (EGF) receptor transinactivation and EGF receptor-independent stimulation of mitogen-activated protein kinase by bradykinin in A431 cells." Biochemical Journal 347, no. 2 (2000): 441–47. http://dx.doi.org/10.1042/bj3470441.

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Transactivation of the epidermal growth factor (EGF) receptor (EGFR) has been proposed to represent an essential link between G-protein-coupled receptors and the mitogen-activated protein kinase (MAPK) pathway in various cell types. In the present work we report, in contrast, that in A431 cells bradykinin transinactivates the EGFR and stimulates MAPK activity independently of EGFR tyrosine phosphorylation. Both effects of bradykinin are mediated by a pertussis-toxin-insensitive G-protein. Three lines of evidence suggest the activation of a protein tyrosine phosphatase (PTP) by bradykinin: (i)

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Lebrun, Ivo, Olga B. Henriques, Fabiana L. A. S. Lebrun, Adriana K. Carmona, Luiz Juliano та Antonio C. M. Camargo. "Isolation and characterization of a new bradykinin potentiating octapeptide from γ-casein". Canadian Journal of Physiology and Pharmacology 73, № 1 (1995): 85–91. http://dx.doi.org/10.1139/y95-012.

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Peptides that display bradykinin-potentiating activity have been obtained from a number of distinct sources, such as snake venoms, fibrinogen, and casein. This paper describes the isolation and sequencing of a novel bradykinin-potentiating peptide, generated by tryptic hydrolysis of the γ-casein chain. No homology was found to other known vasoactive or vasopotentiating peptides. The octapeptide Tyr-Pro-Val-Gln-Pro-Phe-Thr-Glu, corresponding to the γ-casein(114–121) sequence, was isolated from the tryptic hydrolysis of γ-casein and also synthesized by solid-phase peptide synthesis. Both natural

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Santiago, J. A., E. A. Garrison, and P. J. Kadowitz. "Analysis of responses to bradykinin: effects of Hoe-140 in the hindquarters vascular bed of the cat." American Journal of Physiology-Heart and Circulatory Physiology 267, no. 2 (1994): H828—H836. http://dx.doi.org/10.1152/ajpheart.1994.267.2.h828.

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The mechanisms and receptor subtype mediating vasodilator responses to bradykinin were investigated in the hindquarters vascular bed of the cat under constant flow conditions. Intraarterial injections of bradykinin in doses of 10–1,000 ng into the hindquarters vascular bed caused dose-related decreases in perfusion pressure that were inhibited by Hoe-140, a bradykinin B2-receptor antagonist. Injections of des-Arg9-bradykinin (in doses 10-fold higher than for bradykinin) caused smaller dose-related decreases in hindquarters perfusion pressure that were not blocked by Hoe-140. Administration of

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Yokoyama, S., and J. N. Benoit. "Effects of bradykinin on lymphatic pumping in rat mesentery." American Journal of Physiology-Gastrointestinal and Liver Physiology 270, no. 5 (1996): G752—G756. http://dx.doi.org/10.1152/ajpgi.1996.270.5.g752.

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The effects of bradykinin on lymphatic pump activity of rat mesenteric collecting duct were studied, and the receptor subtype responsible for the bradykinin response was evaluated. Rats were anesthetized with intraperitoneal alpha-chloralose and urethan, and exteriorized mesenteries were studied using intravital microscopic techniques. The diameter of the collecting lymph vessels (approximately 100 microns) was continuously monitored and lymphatic pump parameters (end diastolic diameter, end systolic diameter, stroke volume index, ejection fraction, contraction frequency, and pump flow index)

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Ignarro, L. J., R. E. Byrns, G. M. Buga, and K. S. Wood. "Mechanisms of endothelium-dependent vascular smooth muscle relaxation elicited by bradykinin and VIP." American Journal of Physiology-Heart and Circulatory Physiology 253, no. 5 (1987): H1074—H1082. http://dx.doi.org/10.1152/ajpheart.1987.253.5.h1074.

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The objective of this study was to elucidate the mechanisms by which bradykinin and vasoactive intestinal polypeptide (VIP) relax bovine intrapulmonary artery and bradykinin, but not VIP, relaxes intrapulmonary vein. Bradykinin and VIP elicited entirely endothelium-dependent relaxation of phenylephrine-precontracted arterial rings, and this was associated with arterial accumulation of both guanosine 3',5'-cyclic monophosphate (cGMP) and adenosine 3',5'-cyclic monophosphate (cAMP). Bradykinin, but not VIP, relaxed precontracted venous rings and increased cGMP, but not cAMP levels, by endotheliu

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Majumder, Syamantak, Ravi Gupta, Himabindu Reddy, et al. "Cadmium attenuates bradykinin-driven nitric oxide production by interplaying with the localization pattern of endothelial nitric oxide synthase." Biochemistry and Cell Biology 87, no. 4 (2009): 605–20. http://dx.doi.org/10.1139/o09-018.

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Cadmium, a ubiquitous heavy metal, interferes with endothelial functions and angiogenesis. Bradykinin is a Ca-mobilizing soluble peptide that acts via nitric oxide to promote vasodilation and capillary permeability. The objective of the present study was to explore the Cd implications in bradykinin-dependent endothelial functions. An egg yolk angiogenesis model was employed to evaluate the effect of Cd on bradykinin-induced angiogenesis. The results demonstrate that 100 nmol/L Cd attenuated bradykinin-dependent angiogenesis. The results of the in vitro wound healing and tube formation assays b

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Rollins, Korynne S., Joshua R. Smith, Peter J. Esau, Evan A. Kempf, Tyler D. Hopkins, and Steven W. Copp. "Bradykinin does not acutely sensitize the reflex pressor response during hindlimb skeletal muscle stretch in decerebrate rats." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 313, no. 4 (2017): R463—R472. http://dx.doi.org/10.1152/ajpregu.00187.2017.

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Hindlimb skeletal muscle stretch (i.e., selective activation of the muscle mechanoreflex) in decerebrate rats evokes reflex increases in blood pressure and sympathetic nerve activity. Bradykinin has been found to sensitize mechanogated channels through a bradykinin B2 receptor-dependent mechanism. Moreover, bradykinin B2 receptor expression on sensory neurons is increased following chronic femoral artery ligation in the rat (a model of simulated peripheral artery disease). We tested the hypothesis that injection of bradykinin into the arterial supply of a hindlimb in decerebrate, unanesthetize

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Merker, Marilyn P., Said H. Audi, Becky M. Brantmeier, et al. "Proline in vasoactive peptides: consequences for peptide hydrolysis in the lung." American Journal of Physiology-Lung Cellular and Molecular Physiology 276, no. 2 (1999): L341—L350. http://dx.doi.org/10.1152/ajplung.1999.276.2.l341.

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To examine the hypothesis that trans isomers of bradykinin and [Gly6]bradykinin are preferentially hydrolyzed by lung peptidases, we studied the fractional inactivation of these peptides in the perfused rat lung using a bioassay after a single-pass bolus injection and high-performance liquid chromatography after lung recirculation. In the bioassay studies, when the peptides passed through the lung, 25.6-fold more bradykinin or 7-fold more [Gly6]bradykinin was required to elicit a contraction equivalent to that produced when the peptides did not pass through the lung. In the recirculation studi

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Nerdrum, T., D. G. Baker, H. M. Coleridge, and J. C. Coleridge. "Interaction of bradykinin and prostaglandin E1 on cardiac pressor reflex and sympathetic afferents." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 250, no. 5 (1986): R815—R822. http://dx.doi.org/10.1152/ajpregu.1986.250.5.r815.

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Bradykinin applied to the epicardium stimulates cardiac sympathetic afferents and evokes a reflex increase in arterial blood pressure. In anesthetized cats we examined the potentiation of these effects by prostaglandin E1 (PGE1) applied to the ventricular epicardium. We recorded cardiac afferent impulses from the second to the fifth left thoracic sympathetic rami. PGE1 (0.1 microgram/ml) alone had little effect on blood pressure, but it significantly increased the pressor response to bradykinin, and it reduced or abolished tachyphylaxis to repeated applications of bradykinin. Both mechanosensi

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Sun, Ding-Ping, Yuan-Wen Lee, Jui-Tai Chen, Yung-Wei Lin та Ruei-Ming Chen. "The Bradykinin-BDKRB1 Axis Regulates Aquaporin 4 Gene Expression and Consequential Migration and Invasion of Malignant Glioblastoma Cells via a Ca2+-MEK1-ERK1/2-NF-κB Mechanism". Cancers 12, № 3 (2020): 667. http://dx.doi.org/10.3390/cancers12030667.

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Glioblastoma multiforme (GBM) is the most common form of brain tumor and is very aggressive. Rapid migration and invasion of glioblastoma cells are two typical features driving malignance of GBM. Bradykinin functionally prompts calcium influx via activation of bradykinin receptor B1/B2 (BDKRB1/2). In this study, we evaluated the roles of bradykinin in migration and invasion of glioblastoma cells and the possible mechanisms. Expressions of aquaporin 4 (AQP4) mRNA and protein were upregulated in human glioblastomas. Furthermore, exposure of human U87 MG glioblastoma cells to bradykinin specifica

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Maruo, Keishi, Takaaki Akaike, Tomomichi Ono, and Hiroshi Maeda. "Involvement of Bradykinin Generation in Intravascular Dissemination of Vibrio vulnificus and Prevention of Invasion by a Bradykinin Antagonist." Infection and Immunity 66, no. 2 (1998): 866–69. http://dx.doi.org/10.1128/iai.66.2.866-869.1998.

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ABSTRACT Involvement of bradykinin generation in bacterial invasion was examined by using a gram-negative bacillus, Vibrio vulnificus, which is known to invade the blood circulatory system and cause septicemia. V. vulnificus was injected intraperitoneally (i.p.) into mice with or without bradykinin or a bradykinin (B2 receptor) antagonist. Dissemination of V. vulnificus from peritoneal septic foci to the circulating blood was assessed by counting of viable bacteria in venous blood by use of the colony-forming assay. Intravascular dissemination of V. vulnificus in mice was significantly potenti

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Schaffel, Rony, Mozart S. Rodrigues, and Jamil Assreuy. "Potentiation of bradykinin effects and inhibition of kininase activity in isolated smooth muscle." Canadian Journal of Physiology and Pharmacology 69, no. 7 (1991): 904–8. http://dx.doi.org/10.1139/y91-137.

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Prolongation of bradykinin half-life following kininase inhibition has been proposed as the reason for the potentiation of kinin effects. We have reassessed this assumption by using three different isolated smooth muscle preparations and simultaneously studying the inhibition of kininase activity and the potentiation of bradykinin effects by enalaprilat and BPP9a. Rat duodenum displayed higher total kininase activity, metabolizing half of the added bradykinin in 6.5 min, while this time for rat uterus was greater than 60 min. Guinea-pig ileum showed the intermediate value of 14.6 min. Enalapri

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Gao, X. P., J. M. Conlon, J. K. Vishwanatha, R. A. Robbins, and I. Rubinstein. "Loop diuretics attenuate bradykinin-induced increase in clearance of macromolecules in the oral mucosa." Journal of Applied Physiology 80, no. 3 (1996): 818–23. http://dx.doi.org/10.1152/jappl.1996.80.3.818.

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The purpose of this study was to determine whether loop diuretics attenuate bradykinin-induced increase in clearance of macromolecules in the oral mucosa in situ and, if so, to start to determine the mechanisms that mediated these responses. By using intravital microscopy, we found that bradykinin induced a significant concentration-dependent increase in fluorescein isothiocyanate-labeled dextran (mol mass 70 kDa) leaky site formation in the hamster cheek pouch. These responses were significantly attenuated by topical application of two structurally distinct loop diuretics, furosemide and etha

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Beierwaltes, W. H. "Prostaglandin independence of kinin-stimulated renin release." American Journal of Physiology-Renal Physiology 252, no. 5 (1987): F794—F799. http://dx.doi.org/10.1152/ajprenal.1987.252.5.f794.

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Bradykinin can increase prostaglandin synthesis and also stimulate renin release in vitro. Because prostaglandins also stimulate renin, studies were performed to determine whether bradykinin stimulation of renin is a function of prostaglandin synthesis. Isolated glomeruli with attendant arteriolar attachments were harvested from rat kidneys and superfused. The effluent was analyzed for renin, prostaglandins E2 and I2 (6-keto-PGF1 alpha). Bradykinin (10(-5) M) increased renin by 50% with a concomitant increase in prostacyclin (PGI2) but not in prostaglandin E2 (PGE2). The cyclooxygenase inhibit

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Jones, T. H., B. L. Brown, and P. R. M. Dobson. "Bradykinin stimulates phosphoinositide metabolism and prolactin secretion in rat anterior pituitary cells." Journal of Molecular Endocrinology 2, no. 1 (1989): 47–53. http://dx.doi.org/10.1677/jme.0.0020047.

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ABSTRACT Bradykinin stimulated prolactin secretion from monolayer cultures of rat anterior pituitary cells, the stimulation being greater from the cells of male rats. This stimulated secretion was accompanied by a rise in total inositol phosphate accumulation, suggesting that the action of bradykinin is mediated by phosphoinositide hydrolysis. The increase in inositol phosphate accumulation was biphasic; a further sharp rise occurred when the concentration of bradykinin exceeded 1 μmol/l. This may indicate that bradykinin acts on other cell types in the pituitary gland. Bradykinin had no effec

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Brown, Nancy J., John H. Nadeau, and Douglas E. Vaughan. "Selective Stimulation of Tissue-Type Plasminogen Activator (t-PA) In Vivo by Infusion of Bradykinin." Thrombosis and Haemostasis 77, no. 03 (1997): 522–25. http://dx.doi.org/10.1055/s-0038-1656000.

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SummaryAngiotensin converting inhibitors (ACEI) not only decrease angiotensin II (Ang II) but also potentiate the effects of bradykinin. Bradykinin is a potent stimulus to tissue type plasminogen activator (t-PA) secretion in animal models. In this study, we tested the hypothesis that bradykinin increases t-PA levels in humans.Bradykinin was infused in seventeen hypertensive patients randomized to treatment with the ACEIs captopril and quinapril or with placebo. Bradykinin caused a significant decrease in mean arterial pressure (MAP) (p = 0.014) and increase in pulse (p <0.001). ACEI signif

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Brew, E. C., M. B. Mitchell, T. F. Rehring, et al. "Role of bradykinin in cardiac functional protection after global ischemia-reperfusion in rat heart." American Journal of Physiology-Heart and Circulatory Physiology 269, no. 4 (1995): H1370—H1378. http://dx.doi.org/10.1152/ajpheart.1995.269.4.h1370.

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We have reported that cardiac preconditioning against ischemia-reperfusion (IR) can be induced by transient ischemia (TI) and alpha 1-adrenoreceptor stimulation, both mediated by protein kinase C (PKC) (Mitchell, M., X. Meng, C. Parker, E. Brew, A. Harken, and A. Banerjee. Circ. Res. 76: 73-81, 1995). Our study objective was to explore the mechanism of endogenous preconditioning and address the role of PKC activation in bradykinin-mediated cardiac functional protection. Isolated rat heart was used to assess the effects of exogenous bradykinin, TI, selective B2-receptor blocker, and PKC antagon

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Stebbins, C. L., R. C. Smith, and J. C. Longhurst. "Effect of prostaglandins on bradykinin-induced visceral-cardiac reflexes." American Journal of Physiology-Heart and Circulatory Physiology 249, no. 1 (1985): H155—H163. http://dx.doi.org/10.1152/ajpheart.1985.249.1.h155.

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We examined the effect of prostaglandins on the reflex cardiovascular response to bradykinin applied to the abdominal organs of anesthetized cats. Bradykinin (10 micrograms/ml) was applied to the serosal surface of the stomach, gallbladder, or jejunum before and after injection of indomethacin (2-10 micrograms/ml iv) and after application of 1 microgram/ml of prostaglandins E1, E2, or F2 alpha (PGE1, PGE2, PGF2 alpha) or prostacyclin (PGI2). In six cats, stimulation of the stomach with bradykinin significantly increased mean arterial pressure (MAP) by 37 +/- 5 (SE) mmHg and maximal dP/dt by 63

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Kopp, U. C., D. M. Farley, and L. A. Smith. "Bradykinin-mediated activation of renal sensory neurons due to prostaglandin-dependent release of substance P." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 272, no. 6 (1997): R2009—R2016. http://dx.doi.org/10.1152/ajpregu.1997.272.6.r2009.

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In anesthetized rats, renal pelvic administration of bradykinin results in a prostaglandin (PG)-dependent increase in afferent renal nerve activity (ARNA). We now measured renal pelvic release of PGE and substance P during renal pelvic administration of bradykinin. Bradykinin increased ARNA and renal pelvic release of PGE by 497 +/- 252 pg/min and substance P. by 10.7 +/- 7.2 pg/min. Renal pelvic perfusion with indomethacin abolished the bradykinin-mediated increase in ARNA and reduced renal pelvic release of PGE and substance P by 76 +/- 11 and 72 +/- 8%, respectively. To examine whether the

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